1. Brain Damage & Neurodegeneration Flashcards

(25 cards)

1
Q

Are the following terms interchangeable?
- brain damage
- brain disease
- brain injury

A

no: however they have strong physiological connections

brain disease - longer term
brain injury - e.g hitting head

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2
Q

What is congenital vs acquired brain injury?

A

congenital: genetic factors that affect neurodevelopment, pre-natal or birth related trauma

acquired: includes silly things we do, can either be traumatic or non-traumatic

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3
Q

What is non-traumatic vs traumatic brain injury?

A

non traumatic: not sudden, includes a range of conditions e.g strokes, infections, tumours, hypoxia/anoxia

traumatic: sudden

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4
Q

What are the two main causes of a stroke?

A
  1. cerebral haemorrhage
  2. cerebral ischaemia
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5
Q

How does cerebral haemorrhage lead to a stroke?

A
  • artery in brain bursts, causing bleeding in surrounding tissue
  • blood shouldn’t come into contact with neutral tissue as it is essentially toxic
  • often results from an aneurism: if spotted before rupture it can sometimes be treated
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6
Q

How does cerebral ischaemia lead to a stroke?

A
  • blood vessel blockage, leading to an interruption of blood supply to part of the brain
  • leads to a lack of oxygen/glucose leads to excitotoxicity and neuronal cell death
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7
Q

What is closed vs open brain injury?

A

closed: no penetration of the skull
- brain floats in cerebrospinal fluid (cushion)
- damage can be diffuse and widespread

open: skull doesn’t remain intact
- objects penetrate skull and enter brain
- bone fragments can also damage brain tissue
- damage can be localised, but other complications e.g bleeding can lead to wider damage

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8
Q

What are examples of brain disease?

A

Neurodegenerative:
- Alzheimer’s
- Parkinson’s

Other:
- epilepsy
- infections
cancer

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9
Q

What is Parkinson’s disease?

A
  • idiopathic: no single cause with no cure
  • relatively common
  • movement disorder: involuntary tremors, less muscle power
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10
Q

What are the symptoms of Parkinson’s disease?

A
  • insufficiency of movement
  • bradykinesia: very slow movements
  • akinesia: no movement
  • increased muscle tone (rigidity)
  • resting tremor
  • shuffling gait and flexed posture
  • mask like expressions
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11
Q

How is dopamine associated with Parkinson’s disease?

A
  • lack of dopamine in the nigrostriatal dopamine pathway found in the basil ganglia
  • 80% of brains dopamine is found in the basil ganglia
  • degeneration of dopaminergic neurons within the substantia nigra
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12
Q

How is the basil ganglia associated with Parkinson’s disease?

A
  • inhibits motor output
  • should let winning motivation take control: doesn’t happen in Parkinson’s as is initiated by dopamine
  • motor output is inhibited: muscles and movement
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13
Q

How can Parkinson’s be treated by enabling the basil ganglia to be off sometimes?

A
  • replace loss of dopamine by…
  • levo dopamince
  • apomorphine
  • deprenyl
  • cannabis: dopamine agonist

can’t just give dopamine as it doesn’t cross the BBB

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14
Q

How can Parkinson’s be treated using surgical approaches?

A
  • lesion: surgically damage the problem structures of the basil ganglia to mess with the activity levels
  • deep brain stimulation: electrical stimulation of the basil ganglia, inhibiting output
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15
Q

What is dementia vs Alzheimer’s?

A

dementia = generic term of memory disorders, personality changes and impaired reasoning

alzheimer’s = a disease that causes dementia, accounts for 2/3 cases of dementia

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17
Q

How does a brain with severe alzheimer’s compare to a ‘healthy’ brain?

A
  • shrinkage
  • enlarged ventricles
18
Q

What are the symptoms of Alzheimer’s?

A
  • main symptom is memory loss
  • selective decline in memory
  • deficits in attention and personality changes
  • intermediate stages: confusion, anxiety, irritability
  • final stages: swallowing and bladder control
19
Q

How does the neuropathology in AD differ?

A
  • build up of amyloid plaques (protein): accumulates compromising the neurons environment
  • come from APP molecule (amyloid precursor protein)
20
Q

What is the genetic risk factors of AD?

A

APP is found on chromosome 21 (downs syndrome)
- genetic forms of AD appear to have early onset
- usually mutations of the APP gene

apoE (Apolipoprotein E)
- risk or protective factor
- 3 common alleles
- E4 = bad
- E2 = good
-

21
Q

What are neurofibrillary tangles (Tau)?

A
  • neurons that have sticks: called microtubules
  • part of the cytoskeleton which keeps a cells shape
  • made up of MAPs (microtubule associated proteins)
  • Tau is a MAP
  • Tau gets into a muddle and tangles leading to clumps
  • this happens inside neurons
22
Q

How have animal models helped us understand AD?

A
  • genetically modify animals: display AD
23
Q

How can AD be treated?

A

not a cure but treating tau, amyloid or apoE can reduce symptoms
- treatment therefore targets loss of neurons that produce/release the NT acetylcholine, which is important for normal cognitive function especially memory

24
Q

What is cholinesterase AchE?

A
  • enzyme that breaks down acetylcholine
  • prevents it to act on neuron s
  • inhibit AchE ajd you prolong the effect of acetylcholine on the neurons
25